Fractional Flow Reserve following Percutaneous Coronary Intervention

Udit Thakur, Nancy Khav, Andrea Comella, Michael Michail, Abdul R Ihdayhid, Eric Poon, Stephen J Nicholls, Brian Ko, Adam J Brown, Udit Thakur, Nancy Khav, Andrea Comella, Michael Michail, Abdul R Ihdayhid, Eric Poon, Stephen J Nicholls, Brian Ko, Adam J Brown

Abstract

Fractional flow reserve (FFR) is routinely used to determine lesion severity prior to percutaneous coronary intervention (PCI). However, there is an increasing recognition that FFR may also be useful following PCI to identify mechanisms leading to restenosis and the need for repeat revascularization. Post-PCI FFR is associated with the presence and severity of stent under-expansion and may help identify peri-stent-related complications. FFR pullback may also unmask other functionally significant lesions within the target vessel that were not appreciable on angiography. Recent studies have confirmed the prognostic utility of performing routine post-PCI FFR and suggest possible interventional targets that would improve stent durability. In this review, we detail the theoretical basis underlying post-PCI FFR, provide practical tips to facilitate measurement, and discuss the growing evidence supporting its use.

Conflict of interest statement

AJB has received consultancy fees from Abbott Vascular and Boston Scientific. ARI has received consulting fees from Boston Scientific and Canon Medical. BK has received research grants for Canon Medical and honorarium from Medtronic, St Jude Medical, and Abbott. SJN has received research support from AstraZeneca, Amgen, Anthera, CSL Behring, Cerenis, Eli Lilly, Esperion, Resverlogix, Novartis, InfraReDx, and Sanofi-Regeneron and is a consultant for Amgen, Akcea, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Kowa, Merck, Takeda, Pfizer, Sanofi-Regeneron, and Novo Nordisk.

Copyright © 2020 Udit Thakur et al.

Figures

Figure 1
Figure 1
(a) Physiological flow through a well-positioned and expanded stent, facilitating re-endothelialization and inhibiting thrombus generation. (b) Poorly deployed stent leads to a region of accelerated flow and high ESS over the stenotic portion of the stent surface, which activates platelets to release vasoactive mediators including adenosine diphosphate. Adenosine phosphate along with downstream low ESS increases the local concentration of activated platelets, leading to increased stent thrombogenicity.
Figure 2
Figure 2
(a) Angiographic image of post-PCI FFR in the distal left main stem and mid-left anterior descending artery (b) Conceptual representation of post-PCI pressure measurements. FFR is calculated as a ratio of distal coronary pressure (Pd) to aortic pressure (Pa). FFR = Pd/Pa. (c) Pressure curve from post-PCI FFR measurement in the patient from part A, displaying pressure drops across the two stents. (a) and (c) are adapted from Ihdayhid et al. [30] with permission. Copyright © 2016, Elsevier.
Figure 3
Figure 3
A simple schematic approach of interpretation of post-PCI FFR.
Figure 4
Figure 4
Use of post-PCI FFR for side branch assessment and optimization. (a) Suboptimal post-PCI FFR in the ramus (side branch) following bifurcation PCI, warranting further intervention. The pressure curve from this FFR measurement can be seen on the right. (b) Following kissing balloon dilation, post-PCI FFR in the ramus is improved.
Figure 5
Figure 5
Illustration of falsely elevated FFR value in the setting of MI4a: (a) Depiction of downstream infarction due to MI4a. FFR calculation through a patient with a normal heart and no evidence of downstream flow limitation. (b) Falsely elevated FFR values may result secondary to MI4a. A falsely elevated FFR value in the setting of MI4A. MI4a limits the maximal achievable hyperemic flow and hence leads to a falsely elevated FFR value.

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